Urbanization and mortality in Britain, c. 1800-50.

In the long-running debate over standards of living during the industrial revolution, pessimists have identified deteriorating health conditions in towns as undermining the positive effects of rising real incomes on the 'biological standard of living'. This article reviews long-run historical relationships between urbanization and epidemiological trends in England, and then addresses the specific question: did mortality rise especially in rapidly growing industrial and manufacturing towns in the period c. 1830-50? Using comparative data for British, European, and American cities and selected rural populations, this study finds good evidence for widespread increases in mortality in the second quarter of the nineteenth century. However, this phenomenon was not confined to 'new' or industrial towns. Instead, mortality rose in the 1830s especially among young children (aged one to four years) in a wide range of populations and environments. This pattern of heightened mortality extended between c. 1830 and c. 1870, and coincided with a well-established rise and decline in scarlet fever virulence and mortality. The evidence presented here therefore supports claims that mortality worsened for young children in the middle decades of the nineteenth century, but also indicates that this phenomenon was more geographically ubiquitous, less severe, and less chronologically concentrated than previously argued.Leverhulme Trust (award RPG-2012-803) Wellcome Trust (award no. 103322

Smallholders' and large estates' reaction to changed market conditions 1860–1910

Reduced transport costs and income growth in industrialising European countries changed the market conditions for European farmers in the late nineteenth century. Grain prices fell while dairy prices rose. It has been claimed that these price changes hit large grain farmers with vested interests in grain trade particularly hard, while owner-occupiers and smallholders fared better and with help of developing cooperative associations, came out as successful commercial agriculturalists by switching to intensive branches, foremost dairying. Recent research on the Danish case, shows, however, that change was initiated on large elite estates with long-term dairy traditions. The literature on the Swedish case indicates, that larger farms switched to intensified fodder production quicker than smaller farms did, while in the early twentieth century smaller farms played an un-proportionally large role on the dairy market. Using individual farm data from two East-central Swedish parishes in 1878/80, 1895/96 and 1910/11, it is shown, that larger farms tended to modernise crop rotations and switch towards dairy production earlier than small farms did. Smaller farms caught up, and by 1910 their land use was about as strongly adapted to commercial dairy production as larger farms' land use was.Agrarekonomisk tillväxt eller stagnation i Mälardalen: Regionala produktionsdata 1750-1920. Handelsbankens forskningsstiftelser, P2017-0029:

Early-Life Conditions and Old-Age Mortality in a Comparative Perspective : Nineteenth Century Sweden and Belgium

Kermack et al. (1934) proposed the cohort explanation in their analysis of the aggregated mortality decline in England, Wales, Scotland, and Sweden. Their conclusion was that reductions in the death rates of the various age groups attained at any particular time depended primarily on the individuals’ date of birth, and only indirectly on the particular year under consideration. The essential effects on health and survival of adults and older persons were mainly caused by improvements and beneficial effects on their respective birth cohorts during childhood several decades earlier. Jones (1956) brought up the cohort approach anew and recently it has gained focus again through works in medicine but also in historical demography (Barker 1994; Elo and Preston 1992; Fogel 1994; Fridlizius 1989; Kuh and Ben-Shlomo 1997; Preston et al. 1998; Finch and Crimmins 2004). The plausible causal relationships between early-life experiences and old-age mortality have been discussed, with special attention to intrauterine cellular development and cellular development during early childhood. Robert Fogel (1994) has proposed several plausible causal mechanisms that connect malnutrition in utero and during early life to chronic diseases in later life. These propositions are also supported by the work of Barker (1994, 1995) who suggested that the preconditions for coronary heart disease, hypertension, stroke, diabetes, and chronic thyroiditis are initiated in utero without becoming clinically manifest until much later in life. In contrast, Jones (1956), and later Fridlizius (1989), in his analysis of the aggregated mortality decline in Sweden, proposed that the genesis of disease in later life could be due to exposure to certain infectious diseases in the first years of life. Fridlizius argued that this was caused by life-long reduced immunity, which consequently gave higher general risk of other infectious diseases in later life. The knowledge of the medical mechanisms today seems to be more in favour of permanent retardation of organs due to infections rather than immunological mechanisms (Finch and Crimmins 2004). Either way, it implies that factors other than nutrition are important early-life determinants of mortality in later life, because the outcome of some other important infectious diseases, like smallpox, is almost completely unrelated to the nutritional status of the infected individual (Rotberg and Rabb 1985)